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Melittin induces NSCLC apoptosis via inhibition of miR-183.
- Source :
-
OncoTargets & Therapy . Aug2018, Vol. 11, p4511-4523. 13p. - Publication Year :
- 2018
-
Abstract
- Background: Non-small-cell lung cancer (NSCLC) has one of the highest mortality rates among cancers worldwide, with a poor prognosis. Previous studies have reported that melittin, an active component of apitoxin, exerts anti-inflammatory and antitumor effects via vascular endothelial growth factor or FoxO1. Methods: CCK8, flow cytometry assay and Western blotting were performed to evaluate the effect of melittin on NSCLC. Results: The present study demonstrates that melittin activated caspase-2 by inhibiting miR-183 expression and, thus, induced NSCLC apoptosis in both NCI-H441 cancer cell line assays and an in vivo xenograft model. The results of the cell-based assays showed that melittin (2 µg/mL) robustly suppressed miR-183 expression level and resulted in decreased invasion and migration abilities of NCI-H441 cells. Additionally, a flow cytometry assay and Western blotting showed that melittin induced NSCLC NCI-H441 cell apoptosis along with significant elevation of caspase-2 and Bax, which are regulators of cell apoptosis, and reduced Bcl-2 protein expression compared with dimethyl sulfoxide control. Furthermore, subcutaneous injection of melittin (5 mg/kg) significantly suppressed NSCLC tumor growth compared with vehicle group tumors, determined through tumor size and weight. Conclusion: Taken together, the aforementioned findings contribute to identification of a novel therapeutic target in the treatment of NSCLC, in patients diagnosed with a high expression of miR-183. Moreover, this article provides solid evidence for the inhibitory effect of melittin on NSCLC cancer cell growth. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11786930
- Volume :
- 11
- Database :
- Academic Search Index
- Journal :
- OncoTargets & Therapy
- Publication Type :
- Academic Journal
- Accession number :
- 132658019
- Full Text :
- https://doi.org/10.2147/OTT.S169806